Sexual dimorphism in vasopressin-induced contraction of rat aorta

Stallone, John N.; Crofton, J. T.; Share, Leonard

doi:10.1152/ajpheart.1991.260.2.h453

Cited by 52 publications

(62 citation statements)

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“…Finally, the no-exercise vasoconstrictor responses to PE were significantly lower in female compared with male SHR. These results are consistent with several previous reports (17,32,33,52).…”

Section: Discussionsupporting

confidence: 94%

“…However, the sexually dimorphic AP responses during exercise (Fig. 3) may reflect the well-documented attenuated vasoconstrictor response to catecholamines in females (17,32,33,52). Specifically, the observed sex differences in the AP response to exercise may be related to the relative abundance of estrogen and estrogen receptors.…”

Section: Discussionmentioning

confidence: 97%

“…This is an important question because there are sex differences in vascular function, AP, and vascular reactivity to vasoactive agonists. For example, systemic pressor and vascular responses to PE are higher in males than in females (17,32,33,52). These sex influences are due to local modulators of vascular function.…”

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confidence: 99%

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Postexercise α-adrenergic receptor hyporesponsiveness in hypertensive rats is due to nitric oxide

Rao

Collins

DiCarlo

2002

American Journal of Physiology-Regulatory, Integrative and Comp

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.-We tested the hypothesis that a single bout of dynamic exercise produces a postexercise hypotension (PEH) and ␣ 1-adrenergic receptor hyporesponsiveness in spontaneously hypertensive rats (SHR). The postexercise ␣1-adrenergic receptor hyporesponsiveness is due to an enhanced buffering of vasoconstriction by nitric oxide. Male (n ϭ 8) and female (n ϭ 5) SHR were instrumented with a Doppler ultrasonic flow probe around the femoral artery. Distal to the flow probe, a microrenathane catheter was inserted into a branch of the femoral artery for the infusion of the ␣ 1-adrenergic receptor agonist phenylephrine (PE). A microrenathane catheter was inserted into the descending aorta via the left common carotid artery for measurements of arterial pressure (AP) and heart rate. Dose-response curves to PE (3.8 ϫ 10 Ϫ3 Ϫ 1.98 ϫ 10 Ϫ2 g/kHz) were generated before and after a single bout of dynamic exercise. Postexercise AP was reduced in male (13 Ϯ 3 mmHg) and female SHR (18 Ϯ 7 mmHg). Postexercise vasoconstrictor responses to PE were reduced in males due to an enhanced influence of nitric oxide. However, in females, postexercise vasoconstrictor responses to PE were not altered. Results suggest that nitric oxidemediated ␣1-adrenergic receptor hyporesponsiveness contributes to PEH in male but not female SHR. vascular function; gender; arterial pressure; adrenergic receptors FIFTY MILLION AMERICANS HAVE hypertension or are taking antihypertensive medications (30). The morbidity and mortality associated with cardiovascular disease increase exponentially with increasing levels of arterial pressure (AP) (18). Thus interventions designed to lower AP are being vigorously investigated (13, 51). It is well documented that a single bout of dynamic exercise reduces postexercise AP for several hours (11,20,31). Thus acute exercise may be a safe therapeutic approach for lowering AP in hypertensive individuals.The mechanisms mediating postexercise hypotension (PEH) remain the focus of numerous investigative efforts (7,22,35,55). It is generally accepted that PEH is most often associated with elevations in cardiac output (CO) as well as reductions in peripheral vascular resistance (22,24,35) and sympathetic nerve activity (SNA) (16,22,24,35). The postexercise reduction in peripheral vascular resistance may be due to the reduction in SNA as well as a decreased vascular responsiveness to ␣-adrenergic receptor activation. This is suggested because recent evidence has shown that a single bout of dynamic exercise significantly attenuates the vasoconstrictor response to phenylephrine (PE) in an isolated aortic ring preparation (29) and in the intact conscious normotensive rabbit (28) and rat (45). Furthermore, Halliwill and colleagues (22) reported that sympathetic activity is reduced and the transduction of sympathetic activity into vascular resistance is attenuated after dynamic exercise. These data suggest that the ability of the vasculature to respond to a change in SNA or a sustained catecholamine increase after exercise is significantly re...

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Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 97%

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Postexercise α-adrenergic receptor hyporesponsiveness in hypertensive rats is due to nitric oxide

Rao

Collins

DiCarlo

2002

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Again, aorta from male rats showed the greatest sensitivity to NE (Fig. 2), consistent with other studies (12,37). It would appear that alteration by estrogen of the response to NE is complex and cannot be explained in terms of myosin isoform shifts.…”

Section: Discussionsupporting

confidence: 90%

Effects of sex and estrogen on myosin COOH-terminal isoforms and contractility in rat aorta

Rutgeerts

Bowman²,

Johnson³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Paul RJ, Bowman PS, Johnson J, Martin AF. Effects of sex and estrogen on myosin COOH-terminal isoforms and contractility in rat aorta. Am J Physiol Regul Integr Comp Physiol 292: R751-R757, 2007. First published August 17, 2006; doi:10.1152/ajpregu.00167.2006.-We reported that estrogen treatment of ovariectomized rats increased uterine smooth muscle contractility and the ratio of the COOH-terminal myosin heavy chain isoform SM1 (204 kDa) and SM2 [200 kDa; Hewett TE, Martin AF, Paul RJ. J Physiol (Lond) 460: 351-364, 1993]. We extended this model to study sex and estrogen effects on vascular contractility. Experimental groups included 10-to 14-wk-old male (M), female (F), ovariectomized female (OF), and OF treated with estrogen (OF&E) for 7 days with a subcutaneous pellet delivery system, resulting in 17␤-estradiol of 85 (OF&E) vs. 5 (OF or M) pg/ml. The SM1-to-SM2 ratio increased from 1.8 to 2.6 in thoracic aorta, similar to uterine muscle. Isometric force was measured in 5-mm segments of intact and endothelium-denuded (Ϫendo) aorta. With KCl, the maximum forces were in the order OF Ϸ M Ͼ OF&E, and ED50 OF&E Ͼ OF Ϸ M. Differences in ED50 with estrogen persisted after endothelial denudation. The decreased force in Ϫendo OF aorta was not seen in OF&E, suggesting that estrogen altered an endothelium-dependent effect. No differences in maximum forces were noted with norepinephrine: ED50 OF Ͼ OF&E Ͼ M. Estrogen treatment, in contrast to KCl, increased sensitivity. Endothelial denudation increased sensitivity but reduced the differences between groups. With ACh relaxation, males were more sensitive than females, and estrogen had no effect. In the abdominal aorta, there were no changes in SM1/SM2 with 17␤-estradiol, and differences in contractility were blunted. In summary, estrogen treatment decreased responses to KCl but increased sensitivity to norepinephrine; male rats always demonstrated the highest contractility. An increase in the COOH-terminal myosin heavy chain isoform SM1-to-SM2 ratio with 17␤-estradiol treatment may underlie the changes observed in contractility.estrogen; vascular sensitivity; isometric force; myosin isoforms; ovariectomy THE OCCURRENCE OF CARDIOVASCULAR diseases is greater in men aged 30 -50 yr compared with women of similar age (15, 16). The incidence of cardiovascular diseases is also greater in postmenopausal compared with premenopausal women, and vascular protective effects of female sex hormones have been proposed (15,16,18,31). Currently, estrogen replacement therapy to postmenopausal women is in widespread use, but its validity is questioned (14,17,23,27,34,36). The mechanism by which sex and/or estrogen may affect the heart is unknown; it is likely to be multifactorial and has been reviewed in detail (30, 40). Estrogen receptors have been identified on both vascular endothelial (4, 10) and smooth muscle cells (5, 21, 22, 29), providing two potential pathways by which estrogen could affect vascular function. In addition, non-receptor-mediated mechanisms may play a role (35). Estroge...

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“…Contractile responses are greater in the aorta of male than female rats (Stallone et al, 1991;Tostes et al, 2000). These differences may be related to the vasodilatory effects of estrogens Kanashiro & Khalil, 2001) through a direct action on vascular smooth muscle (Jiang et al, 1992;Mugge et al, 1993;Gerhard & Ganz, 1995;.…”

Section: Gender Differences On Vascular Agingmentioning

confidence: 97%